The essential features of this proposal are to study models for iron catalyzed biooxidations with specific interest in the mechanism for hydroxylation of proline in relation to the biosynthesis of collagen. Specific aims include: 1. Determining the mechanism for iron catalyzed a) oxidative decarboxylation of 2-keto carboxylic acids and b) aliphatic oxidations. 2. Establish model reactions to provide chemical precedent and insight into the mechanism of action of prolyl hydroxylase. 3. Evaluate the validity of using biomimicry as a basis for the development of new chemistry. Alterations in the number of hydroxyproline residues in collagen, which arise from changes in the action of prolyl hydroxylase, are suspected to underlie arthritic conditions, atherosclerosis, and the aging process in general. Thus, an understanding of the mechanism for proline hydroxylation should be both physiologically significant and of current medical interest. The results of this work may provide valuable insight for the design of chemotherapeutics useful for the regulation of collagen hydroxylation.